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11 l Lipase ❖Add tartrate buffer: 1. + in pancreatitis ~ Prostatic ACP inhibited by...

11 l Lipase ❖Add tartrate buffer: 1. + in pancreatitis ~ Prostatic ACP inhibited by tartrate 2. Remains elevated longer than amylase I@' RBC ACP not inhibited by tartrate 3. More specific for acute pancreatitis c. Immunoassay for prostatic ACP 4. Methods: 4. Specimen Collection and Handling a. Turbidimetric b. Older method: olive oil substrate; a. Hemolysis results in falsely + results measure fatty acids product b. Storage at room temperature results in loss of enzyme activity; must TE$ remove serum from cells ASAP and stabilize (add disodium citrate t monohydrate or pH to 5.4 with acetic acid) Clinical Significance ofan bicre1JSed Amylase Test Most SpeciJic for Acute Pancreatitis Specimen Handling for Acid Phosphatase Determination ACP (Acid Phosphatase) 1. Sources: primarily prostate; other Cholinesterase tissues: erythrocytes, bone, liver, 1. Erythrocyte acetylcholinesterase and spleen, kidney, platelets plasma pseudocholinesterase 2. Clinical significance 2. Destroys acetylcholine after nerve a. Highest elevations seen in impulse transmission metastasizing carcinoma of prostate; now use PSA instead 3. Severe t results in serious b. + in bone disease or cancers that neuromuscular effects; one of few enzymes in which t is clinically metastasize to hone and in metastasizing breast cancer significant c. Tartrate-resistant portion elevated in hairy cell. leukemia 4. t cholinesterase: organophosphate poisoning and genetic susceptibility to d. Presence in seminal fluid useful in certain anesthetic agents forensic medicine for rape cases; now use PSA instead 3. Methods: a. Spectrophotometric for Total ACP ❖ Phosphate substrate (Ex. p-.nitrophenyl phosphate) Test Helpful in Determining cleaved by ACP to give colored Pesticide Poisoning product (Ex. p-nitrophenol after OH- added; yellow, read at 410nm) Cardiac Markers to Evaluate Possible Acute b. Spectrophotometric for Prostatic Myocardial lnfardion (AMI or Ml) ACP: 1. Myoglobin ❖ Use substrates more specific for a. Produced by muscles including prostatic ACP (Ex. h eart thymolphthalein monophosphate b..+ in muscle damage including AMI and alpha naphthyl phosphate) c. + in renal damage 112 d. Rises within 30 minutes of AMI; g. If BNP given as medication peaks within 4-10 hours and returns (Natreco~) to t blood pressure, to normal within 24 hours must u se NT pro-BNP to monitor e. Absence rules out AMI but ,+. does ventricular BNP release not diagnose AMI because may be h. Also used for risk stratification due to other muscle trauma other Cardiac Risk Assessment Markers 2. CK2 ( CK-MB) 1. hsCRP a. Immunoassays: mass CK2 a ssays a. Sensitive marker for chronic measure concentration rather than inflammation activity b. Pa6ent must b e free of other b. Rises within 6-10 hours of AMI; inflammatory processes (trauma , peaks within 24 hours; returns to rheumatoid arthritis, infection, normal in 2-3 days etc.) c. Replaced by Troponin for detection c. Elevated levels potential risk factor of AMI 2. Homocysteine 3. Troponin a. Amino acid associated with vitamin a. Single best test for diagnosis of AMI B6, Bl2 and folic acid b. Troponin (Tn) is complex of 3 b. Elevated levels potential risk factor muscle fiber proteins: troponin T (Tn1), troponin I (Tnl) and troponin C (Tn C) c. l soforms cTnT and cTnl are very specific to cardiac muscle and either may be u sed for detection of AMI d. cTnT and cTnl often called TnT and Tnl or simply Tn e. Rises 4-8 hours after AMI; peaks at approximately 12-14 hours; r em ains elevated for up to 10 days Liver Markers f. Also used for cardiac risk stratification 1. AST - highest valu es in hepatitis Cardiac Markers to Assess 2. ALT - highest values in hepatitis, liver Congestive Heart Failure sp ecific 1. B-type Natriuretic Peptide (BNP) and 3. LD - found in many tissues other than N-Terminal pro-BNP (NT pro-BNP) liver (ex., h eart, skeletal muscle) a. BNP and NT pro-BNP levels ,+. in congestive heart failure ( CHF) 4. ALP - biliary obstruction; may be ❖ Levels correlate to classification of slightly elevated in hepatitis stages of CHF h. Released by ventricular walls in 5. 5 1 NT - biliary obstruction response to hypertension and volume overload 6. GGT - liver-specific; highest + from c. Pre-pro-BNP cleaved to BNP biliary ob struction or after alcohol (active) and T pro-BNP (inactive) ingestion d. Natriuretic because BNP ,t. Na+ and water excr etion and causes vasodilation to t blood pressure REMEMBER! e. BNP antagonist to renin- Elevated Liver En~mes angiotensin-aldosterone system are as Easy as AB c; (RAAS) which,+. blood pressure by vasoconstriction and r etention of A,lcoholism Na+ and water f. NT pro-BNP cleared b y kidneys so §.iliary Obstruction affected by renal function ~irrhosis  113 REMEMBER! REMEMBER! Hepatitis vs. Muscle Man Obstruction M u AST Adapte